SAN DIEGO, July 16, 2013 – Confirming an enzyme in the serine hyrdrolase family as a therapeutic target to slow and potentially reverse the effects of Down syndrome and Alzheimer’s disease is the goal of new research announced today by Abide Therapeutics, in collaboration with researchers at the University of California, San Diego School of Medicine and funded by a grant from the Cure Alzheimer’s Fund.
BOSTON – New research examining levels of the hallmark proteins linked to Alzheimer's disease found in patients suffering from post-operative cognitive changes (POCC) may lead to safer surgery care and better post-operative outcomes for senior adults.
Research uncovering 12 new gene variations connected to the cause of the early-onset familial form of Alzheimer’s disease (EO-FAD), which generally strikes before the age of 65, is being published in the journal Molecular Psychiatry.
In his heyday, Professor Charles K. Kao was a pioneer in the field of fiber optics. In 2009 he was honored with the Nobel Prize in Physics. Today, at age 79, Kao no longer is able to read or speak, because he suffers from Alzheimer’s disease.
As hard as life is for Gwen Kao, his wife for more than 50 years and primary caregiver, she created The Charles K. Kao Foundation in his honor to raise awareness for the disease and educate the public about what can be done.
While many were anxious to accept initial findings showing a drug known as Targretin’s “too good to be true” lab results with Alzheimer’s disease, subsequent attempts to confirm and replicate the original data regarding the ability of Targretin to remove amyloid plaques, the cardinal lesion of the disease, have largely failed. Cure Alzheimer’s Fund Research Consortium members Dr. Sangram Sisodia, professor of neuroscience at the University of Chicago and Dr.
Cure Alzheimer’s Fund and National Institute of Mental Health Join in Awarding Millions for Whole Genome Sequencing
Henry McCance, chairman emeritus of Greylock Partners, co-founded Cure Alzheimer’s Fund (CAF) in 2005 after getting frustrated with the lack of knowledge about the disease when his wife was diagnosed. He was interviewed by the Boston Business Journal about his venture capital approach to funding Alzheimer's disease research.
BOSTON— Excessive levels of the protein CD33 can impede the clearance of the plaque-forming protein, amyloid beta, the key component of senile plaques in the brains of Alzheimer’s disease patients. The discovery, made by Dr. Rudolph Tanzi and colleagues at Massachusetts General Hospital, and co-funded by the Cure Alzheimer’s Fund and the National Institute of Mental Health (NIMH) will be published in the journal Neuron.
Cure Alzheimer’s Fund is saddened by the terror attack at the Boston Marathon. Our hearts go out to all who have been affected by these horrible incidents. We are so proud of the runners, all those behind the scenes and all who supported our marathon running team this year. We are happy to report that none of our team was near enough to the blasts to be injured. We want to say thank you to those who supported our marathon team. Also thanks to the many of you who have expressed concern.
The study, led by Cure Alzheimer’s Research Consortium member Sam Gandy, M.D., Ph.D., of the Icahn School of Medicine at Mount Sinai, examined how elements in air pollution such as nickel nanoparticles affect the levels of certain peptides in the brain that are found to be at heightened levels in patients suffering from Alzheimer’s Disease.
“We don’t yet completely understand why the peptides accumulate, but we do know the genes responding to the peptides play an important role in developing Alzheimer’s,” said Gandy.
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